Journal
AGEING RESEARCH REVIEWS
Volume 79, Issue -, Pages -Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.arr.2022.101653
Keywords
Ataxia-telangiectasia; ATM; DNA damage response; Cellular senescence; Aging; Mitochondrial dysfunction; Oxidative stress
Categories
Funding
- University of Queensland Early Career Researcher Grant [UQECR2058457]
- NHMRC [APP2001408]
- Brisbane Children's Hospital Foundation [Project-50308]
- Jerome Lejeune Postdoctoral Fellowship - BrAshA-T Foundation
- Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
- Israel Cancer Research Fund
- A-T Children's Project
- US-Israel Binational Science Foundation (BSF)
- ARC Discovery Project [DP210103401]
- Australian NHMRC
- [APP1138795]
- [APP1127976]
- [APP1144806]
- [APP1130168]
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Ataxia-telangiectasia (A-T) is a complex disorder characterized by progressive cerebellar degeneration, immunodeficiency, radiation sensitivity, genome instability, and predisposition to cancer. The premature aging component of A-T is of great importance in driving the disease.
Ataxia-telangiectasia (A-T) is caused by absence of the catalytic activity of ATM, a protein kinase that plays a central role in the DNA damage response, many branches of cellular metabolism, redox and mitochondrial ho-meostasis, and cell cycle regulation. A-T is a complex disorder characterized mainly by progressive cerebellar degeneration, immunodeficiency, radiation sensitivity, genome instability, and predisposition to cancer. It is increasingly recognized that the premature aging component of A-T is an important driver of this disease, and A -T is therefore an attractive model to study the aging process. This review outlines the current state of knowledge pertaining to the molecular and cellular signatures of aging in A-T and proposes how these new insights can guide novel therapeutic approaches for A-T.
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